추천 제품
분석
≥95% (HPLC)
Quality Level
형태
solid
제조업체/상표
Calbiochem®
저장 조건
OK to freeze
protect from light
색상
brown
solubility
DMSO: 50 mg/mL
배송 상태
ambient
저장 온도
2-8°C
InChI
1S/C14H14ClN3S/c15-11-7-5-10(6-8-11)13-9-19-14(16-13)18-17-12-3-1-2-4-12/h5-9H,1-4H2,(H,16,18)
InChI key
YYTHPXHGWSAKIZ-UHFFFAOYSA-N
일반 설명
A cell-permeable thiazolyl-hydrazone compound that inhibits the acetylation of histone H3 by recombinant human Gcn5 in a substrate-competive manner, while exhibiting little activity against rhGcn5 autoacetylation. Although functional knockout of Gcn5 in Saccharomyces cerevisiae by genetic deletion or by CPTH2 treatment is not detrimental to the survival of the budding yeast, CPTH2 treatment is shown to inhibit the growth of yeast strain genetically deleted of Gcn5, but not strains deleted of Elp3 or Sas2.
A cell-permeable thiazolyl-hydrazone compound that inhibits the acetylation of histone H3 by recombinant human Gcn5 in a substrate-competive manner, while exhibiting little activity against rhGcn5 autoacetylation. Although functional knockout of Gcn5 in Saccharomyces cerevisiae by genetic deletion or by CPTH2 treatment is not detrimental to the survival of the budding yeast, CPTH2 treatment is shown to inhibit the growth of yeast strain genetically deleted of Gcn5, but not strains deleted of Elp3 or Sas2.
포장
Packaged under inert gas
경고
Toxicity: Standard Handling (A)
재구성
Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 6 months at -20°C.
기타 정보
Larrieu, D., et al. 2014. Science, 344, 527.
Chimenti, F., et al. 2009. J. Med. Chem.52, 530.
Chimenti, F., et al. 2009. J. Med. Chem.52, 530.
법적 정보
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
Storage Class Code
11 - Combustible Solids
WGK
nwg
Flash Point (°F)
Not applicable
Flash Point (°C)
Not applicable
시험 성적서(COA)
제품의 로트/배치 번호를 입력하여 시험 성적서(COA)을 검색하십시오. 로트 및 배치 번호는 제품 라벨에 있는 ‘로트’ 또는 ‘배치’라는 용어 뒤에서 찾을 수 있습니다.
Cancer research communications, 2(6), 402-416 (2023-01-24)
The emergence of treatment resistance significantly reduces the clinical utility of many effective targeted therapies. Although both genetic and epigenetic mechanisms of drug resistance have been reported, whether these mechanisms are stochastically selected in individual tumors or governed by a
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